Fig. 1

Summary of the various effects of addictive drugs on cellular messenger molecules affecting cognitive impairment. METH induces inflammatory cytokines through TLR, Myd88, and NF-κB pathways. Cannabinoids induces the production of inflammatory cytokines via CB₂. In contrast, cocaine inhibits NF-κB activation. In addition, cocaine induces ROS by increasing glutamate levels. Ketamine interferes with CaMKIIβ and PKA activity as it decreases NMDAR and ultimately blocks CREB activation, thereby reducing neuronal gene transcription. Likewise, METH inhibits CREB activation by upregulating the expression of Drd1 and decreasing ERK 1/2 phosphorylation. METH methamphetamine, TLR Toll-like receptor, NF-κB nuclear factor kappa-B, NMDAR N-methyl-D-aspartate receptor, CaMKIIβ Ca²⁺/calmodulin-dependent protein kinase II, ROS reactive oxygen species, PKA, protein kinase A, CREB cAMP response element-binding protein, ERK1/2, extracellular signal-regulated kinase 1/2, Drd1 dopamine receptor 1